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Am J Physiol Lung Cell Mol Physiol (February 10, 2006). doi:10.1152/ajplung.00327.2005
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Submitted on July 25, 2005
Accepted on February 7, 2006

NKG2D Ligands are Expressed on Stressed Human Airway Epithelial Cells

Michael T Borchers1*, Nathaniel L Harris2, Scott C Wesselkamper1, Mark Vitucci1, and David Cosman3

1 Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH, USA
2 Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, OH, USA; Department of Internal Medicine, College of Medicine, Cincinnati, OH, USA
3 AMGEN Washington, Inc., Seattle, WA, USA

* To whom correspondence should be addressed. E-mail: michael.borchers{at}uc.edu.

Immune surveillance of the airways is critical to maintain the integrity and health of the lung. We have identified a family of ligands expressed on the surface of stressed airway epithelial cells whose function is to bind the NKG2D activating receptor found on several pulmonary lymphocytes including natural killer cells, {gamma}{delta}+ T cells, and CD8+ T cells. We employed real-time PCR and flow cytometry in normal and transformed airway epithelial cell to demonstrate that MICB and the ULBP ligands (ULBP1-4) are ubiquitously expressed at the mRNA level in all cell lines. MICA/B surface expression was present on 70% of transformed cell lines but was undetectable on primary cells. We demonstrate that MICA/B, and ULBP1, 2, 3, and 4 expression is rare or absent on the cell surface of unstimulated normal human bronchial epithelial cells although transcripts and intracellular proteins are present. NHBE cells exposed to 0.3mM hydrogen peroxide exhibit an induction of all ligands examined on the cell surface. Surface expression is independent of changes in transcript level or total cellular protein and is mediated the ERK family of mitogen-activated protein kinases. The induction of NKG2D ligands on stressed airway epithelial cells represents a potentially important mechanism of immune cell activation in regulation of pulmonary health and disease.




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